European Journal of Cardiovascular Medicine

Metabolic Syndrome (MetS) represents a cluster of interrelated cardiometabolic abnormalities defined by central obesity, hyperglycemia, dyslipidemia, and hypertension, which collectively increase the risk of type 2 diabetes mellitus (T2DM), cardiovascular disease (CVD), and overall mortality. In recent decades, the prevalence of MetS has risen dramatically worldwide, parallel to the global epidemics of obesity and sedentary lifestyle. The syndrome affects approximately one-quarter of the world’s adult population, with variations depending on age, sex, ethnicity, and lifestyle factors. The International Diabetes Federation (IDF) and the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) remain the most widely used definitions for MetS, consistently underscoring abdominal obesity and insulin resistance as central pathophysiological drivers. Non-Alcoholic Fatty Liver Disease (NAFLD), defined as ≥5% hepatic steatosis in the absence of significant alcohol consumption, viral hepatitis, or other specific causes of liver fat accumulation, has emerged as the most common chronic liver disease globally. Current estimates suggest that NAFLD affects nearly one-third of the adult population, with even higher prevalence reported in individuals with obesity, diabetes, and other metabolic risk factors.^[1][2]

MetS and NAFLD share a common pathophysiological basis rooted in insulin resistance, chronic low-grade inflammation, adipocyte dysfunction, and ectopic lipid deposition. As a result, NAFLD is increasingly being recognized as the hepatic manifestation of MetS. Numerous epidemiological studies have demonstrated that the presence and severity of NAFLD are strongly associated with the number of MetS components, particularly abdominal obesity, hypertriglyceridemia, and impaired glucose metabolism. The progression of NAFLD from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and hepatocellular carcinoma is significantly influenced by the metabolic milieu created by MetS. Thus, early identification of individuals with MetS and concurrent NAFLD is essential for risk stratification and implementation of targeted lifestyle and pharmacological interventions.^[3][4]

In resce-limited settings, ultrasonography remains the most practical and cost-effective tool for detecting hepatic steatosis, while biochemical parameters such as fasting glucose, lipid profile, and anthropometric measurements allow simple assessment of MetS. The rising burden of NAFLD in India, particularly among adults with sedentary lifestyle patterns and increasing adiposity, highlights the need for population-level epidemiological studies. Despite growing evidence linking MetS with NAFLD, regional variations in prevalence and demographic patterns necessitate localized research to guide preventive strategies and health-care planning.^[5]

Aim

To determine the prevalence of metabolic syndrome and assess its association with non-alcoholic fatty liver disease among adults in a tertiary-care setting.

Objectives

1. To estimate the prevalence of metabolic syndrome in adults aged ≥18 years.
2. To determine the prevalence and grading of NAFLD using abdominal ultrasonography.
3. To evaluate the association between components of metabolic syndrome and the presence of NAFLD.

Sce of Data

Data were obtained from adult patients attending the outpatient and inpatient departments of the tertiary-care hospital during the study period. Clinical, anthropometric, biochemical, and ultrasonographic data were collected prospectively using a structured proforma.

Study Design

The study was a hospital-based cross-sectional analytical study.

Study Location

The study was conducted at the Department of General Medicine in a tertiary-care medical college hospital.

Study Duration

The study was carried out over a period of 12 months from January 2022 to December 2022.

Sample Size

A total of 200 adult participants (≥18 years) were included.

Inclusion Criteria

• Adults aged 18 years and above.
• Individuals who provided written informed consent.
• Participants undergoing ultrasonography for routine evaluation or metabolic screening.

Exclusion Criteria

• History of significant alcohol intake (>20 g/day for women, >30 g/day for men).
• Known cases of viral hepatitis (HBV, HCV), autoimmune liver disease, drug-induced liver injury, or genetic liver disorders.
• Pregnant women.
• Patients with incomplete clinical or laboratory data.

Procedure and Methodology

All eligible participants were screened, and demographic data including age, sex, occupation, lifestyle factors, and medical history were recorded. Anthropometric measurements included height, weight, waist circumference, and body mass index (BMI). Blood pressure was measured using a standardized protocol. Fasting blood samples were collected after an overnight fast of 8-12 hs. Biochemical parameters included fasting plasma glucose, serum triglycerides, HDL-cholesterol, and liver function tests. Metabolic Syndrome was diagnosed based on the NCEP ATP III criteria. Ultrasonography of the abdomen was performed by a trained radiologist using a high-resolution B-mode ultrasound machine. NAFLD was graded based on standard echogenic criteria into Grade 0-III steatosis. All findings were entered into a predesigned data collection sheet.

Sample Processing

Blood samples were centrifuged, and serum was analyzed using automated analyzers. Quality control procedures were strictly followed according to laboratory standards.

Statistical Methods

Data were entered into Microsoft Excel and analyzed using SPSS software (version 27.0). Descriptive statistics such as mean, standard deviation, and proportions were calculated. The association between MetS and NAFLD was assessed using chi-square test, odds ratios, and logistic regression. A p-value <0.05 was considered statistically significant.

Data Collection

Data were collected using a structured proforma that included demographic details, clinical history, anthropometric readings, biochemical results, and ultrasound findings. All patient data were coded to maintain confidentiality

Table 1: Overall prevalence of Metabolic Syndrome and NAFLD and their crude association (N = 200)

Table 1 illustrates the overall prevalence of metabolic syndrome (MetS) and non-alcoholic fatty liver disease (NAFLD) in the study population (N = 200) and evaluates their crude association. Metabolic syndrome was present in 94 participants, accounting for 47.0% of the population, with a 95% confidence interval (CI) ranging from 40.1% to 53.9%. A one-sample z-test comparing this proportion with a hypothesized prevalence of 50% showed no statistically significant deviation (z = −0.85; p = 0.40). NAFLD was identified in 88 participants (44.0%, 95% CI: 37.1%-50.9%), which also did not significantly differ from the reference value of 50% (z = −1.70; p = 0.09). However, a strong crude association was observed between MetS and NAFLD. Among individuals with MetS, 67.0% (63/94) had NAFLD, compared with only 23.6% (25/106) of those without MetS. This difference was highly significant, with a risk ratio of 2.84 (95% CI: 1.96-4.12) and a chi-square statistic of χ²(1) = 38.15 (p < 0.001).

Table 2: Baseline characteristics by metabolic syndrome status (N = 200)

Table 2 compares baseline demographic, anthropometric, and biochemical characteristics between individuals with and without metabolic syndrome. Participants with MetS were significantly older (49.3 ± 10.4 years) than those without MetS (43.8 ± 11.2 years), with a mean difference of 5.5 years (95% CI: 2.51-8.49; p = 0.0003). Marked differences were observed in adiposity measures: individuals with MetS had substantially higher BMI (29.1 ± 3.4 vs 25.7 ± 3.6 kg/m²; mean difference: 3.4 kg/m²; p < 0.001) and waist circumference (98.6 ± 8.9 vs 88.3 ± 9.4 cm; mean difference: 10.3 cm; p < 0.001). MetS participants also demonstrated significantly higher systolic blood pressure (138.7 ± 14.2 vs 124.6 ± 13.8 mmHg; p < 0.001) and fasting plasma glucose levels (118.3 ± 23.4 vs 96.2 ± 17.6 mg/dL; p < 0.001). Dyslipidemia was more pronounced in the MetS group, as reflected by elevated triglyceride levels (192.6 ± 54.8 vs 138.7 ± 46.1 mg/dL; p < 0.001) and lower HDL cholesterol (39.4 ± 7.1 vs 46.8 ± 8.3 mg/dL; p < 0.001). Sex distribution did not significantly differ between groups, with females comprising 55.3% of the MetS group versus 46.2% of the non-MetS group (RR = 1.20; p = 0.20).

Table 3: Prevalence and grading of NAFLD by ultrasonography (N = 200)

Table 3 presents the prevalence and grading of NAFLD based on ultrasonographic assessment. NAFLD was present in 44.0% (88/200) of adults, whereas 56.0% (112/200) showed no fatty infiltration. Among NAFLD cases, Grade 1 steatosis was the most common form, accounting for 24.5% of the total population, followed by Grade 2 (13.5%) and Grade 3 (6.0%). The 95% CIs around these proportions confirm the precision of estimates, and no inferential statistics were required for graded categories. A significant trend was observed when comparing serum ALT levels across NAFLD grades. Mean ALT levels increased progressively from 28.6 ± 9.7 U/L in participants without NAFLD to 42.3 ± 13.9 U/L in Grade 1, 61.8 ± 19.4 U/L in Grade 2, and 79.4 ± 24.1 U/L in Grade 3. One-way ANOVA demonstrated a highly significant difference in ALT values across the f groups (F ≈ 42.3, p < 0.001).

Table 4: Association between components of Metabolic Syndrome and NAFLD (N = 200)

Table 4 evaluates the association between individual components of metabolic syndrome and the presence of NAFLD. Central obesity showed a strong and statistically significant association with NAFLD, with 58.5% of obese individuals exhibiting fatty liver compared to 20.8% of those without central obesity (RR = 2.82; 95% CI: 1.78-4.47; p < 0.001). Elevated triglycerides were also significantly associated with NAFLD, with affected individuals demonstrating more than double the risk (RR = 2.10; p < 0.001). Low HDL cholesterol exhibited the strongest association, where 60.7% of individuals with reduced HDL had NAFLD compared to 20.5% without this abnormality (RR = 2.96; 95% CI: 1.89-4.64; p < 0.001). Elevated blood pressure (RR = 2.22; p < 0.001) and elevated fasting glucose (RR = 2.25; p < 0.001) were likewise strongly associated with NAFLD.

In the present study, the prevalence of metabolic syndrome (MetS) among adults attending a tertiary-care hospital was 47.0%, while NAFLD, diagnosed by ultrasonography, was observed in 44.0% of participants (Table 1). These figures are higher than the global pooled prevalence estimates of NAFLD of about 25-30% reported by Mascaró CM et al. (2022)^[6], who highlighted NAFLD as a major cause of chronic liver disease worldwide. NAFLD prevalence lies within the wide Indian range (9-49.8%) summarized by Younossi ZM et al. (2019)^[7], who also noted that the prevalence of MetS in Indian adults is approximately 30% and rising in parallel with diabetes and obesity. The slightly higher prevalence of both MetS and NAFLD in cohort could be explained by the hospital-based sampling of high-risk individuals, compared with community-based screening in some population studies.

The crude association between MetS and NAFLD in study was strong: 67.0% of participants with MetS had NAFLD compared with 23.6% of those without MetS, corresponding to a risk ratio (RR) of 2.84 (95% CI: 1.96-4.12; p < 0.001) (Table 1). This strong link aligns with the concept of NAFLD as the hepatic manifestation of MetS. Studies from Europe and Asia have reported similar magnitudes of association. Lim S et al. (2021)^[8] found an ultrasound-diagnosed NAFLD prevalence of 40% in an internal medicine cohort and noted higher MetS burden among those with fatty liver. In a rural north Indian population, an outpatient-based study reported NAFLD prevalence of 18.8%; importantly, metabolic syndrome was significantly more frequent among NAFLD subjects (42.7%) than controls (17.9%), reinforcing the clustering of metabolic abnormalities with hepatic steatosis (MSJ study, western Uttar Pradesh) as described by the Jinjuvadia R et al. (2017)^[9]. observed RR of 2.84 is very similar to that reported in a tertiary-care study from south India, where NAFLD was present in 42.6% of patients with MetS versus 21.3% without MetS, with an overall NAFLD prevalence of 32.0% Zakerkish M et al. (2021)^[10].

Table 2 shows that subjects with MetS in cohort had a clearly adverse cardiometabolic profile compared with those without MetS, with significantly higher mean age, BMI, waist circumference, systolic blood pressure, fasting plasma glucose and triglycerides, and significantly lower HDL cholesterol. These findings are consistent with the pathophysiological framework described by Pastori D et al. (2021)^[11], who emphasized abdominal obesity, insulin resistance, hypertriglyceridaemia and low HDL-C as central drivers linking NAFLD and MetS. The magnitude of differences in BMI and waist circumference observed in data (≈3-10 units higher in the MetS group) is comparable to other Indian hospital-based series, where subjects with NAFLD or MetS also had substantially higher anthropometric and glycaemic indices. In the south Indian NAFLD-MetS study cited above, mean age was around 50 years in the MetS group, similar to MetS mean age of 49.3 years, and NAFLD prevalence rose steeply with increasing BMI and waist circumference. Likewise, an Iranian cohort of NAFLD patients studied by Muzurović E et al. (2021)^[12] reported MetS in about two-thirds of NAFLD subjects, who had significantly higher BMI, waist circumference and fasting glucose than non-MetS individuals, mirroring the pattern we observed.

Regarding NAFLD severity, Table 3 indicates that 24.5% of all participants had Grade 1 steatosis, 13.5% had Grade 2, and 6.0% had Grade 3, while 56.0% had no fatty liver. This distribution with Grade 1 as the predominant category followed by lower proportions of Grades 2 and 3 is similar to ultrasonographic patterns reported from both European and Indian cohorts. et al. (20)^[3] observed an NAFLD prevalence of 40% in a German cohort with most cases in the mild-to-moderate range, while Lim S et al. (2021)^[8] from an urban Indian setting also reported a high burden of ultrasound-detected NAFLD, with most subjects clustering in grades 1 and 2^[6]. In study, serum ALT levels rose progressively and significantly across NAFLD grades (ANOVA F ≈ 42.3; p < 0.001), supporting a dose-response relationship between steatosis severity and hepatocellular injury. This trend is in concordance with pooled data from NAFLD epidemiology reviews, where higher ALT and AST values have been consistently associated with more advanced steatosis and fibrosis, even though a proportion of NAFLD patients may have “normal” transaminases.

Table 4 further dissects the association between individual MetS components and NAFLD. Central obesity, elevated triglycerides, low HDL cholesterol, elevated blood pressure and elevated fasting glucose all showed significant and independent associations with NAFLD, with risk ratios ranging from approximately 2.10 to 2.96 and p-values <0.001. Central obesity (RR 2.82) and low HDL-C (RR 2.96) emerged as particularly strong correlates. These findings mirror those of several Indian and international studies. A study from north India examining NAFLD and MetS components at a tertiary centre in Uttarakhand reported significantly higher frequencies of abdominal obesity, hypertriglyceridaemia, low HDL-C, hypertension and impaired fasting glucose among NAFLD subjects, with particularly strong associations for waist circumference and low HDL Muzurović E et al. (2021)^[12]. Similarly, study by Younossi ZM et al. (2019)^[7] found that approximately 65-66% of NAFLD patients met MetS criteria, with each additional MetS component substantially increasing NAFLD risk.

The present cross-sectional study demonstrated a high prevalence of both Metabolic Syndrome (47%) and Non-Alcoholic Fatty Liver Disease (44%) among adults attending a tertiary-care hospital. A strong and statistically significant association was observed between MetS and NAFLD, with individuals having MetS nearly three times more likely to exhibit fatty liver compared to those without MetS. Central obesity, hypertriglyceridemia, low HDL cholesterol, elevated blood pressure, and impaired fasting glucose emerged as key metabolic components independently associated with NAFLD, reinforcing the shared pathophysiological basis of these conditions. The progressive rise in ALT levels across increasing NAFLD grades further underscores the hepatic impact of metabolic derangements. Overall, the findings highlight the urgent need for early identification, lifestyle modification, and targeted interventions in individuals with metabolic risk factors to prevent progression to advanced liver disease and reduce future cardiometabolic complications.

LIMITATIONS

This study has several limitations.

1. Hospital-based design: The participants were recruited from a tertiary-care setting, which may overrepresent individuals with existing metabolic risk factors, limiting the generalizability of findings to the general population.
2. Cross-sectional nature: Causality between MetS and NAFLD cannot be established, as temporal relationships were not assessed.
3. Ultrasound-based diagnosis: NAFLD was diagnosed using ultrasonography, which, although practical and widely used, has limited sensitivity for detecting mild steatosis and cannot distinguish steatohepatitis or assess fibrosis severity.
4. Unmeasured confounders: Dietary factors, physical activity, genetic markers, and socioeconomic parameters were not evaluated, which may influence both metabolic syndrome and NAFLD risk.
5. Single-center study: Results may not reflect regional or national diversity in metabolic and liver disease patterns.

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